Independent of the disease type, high hemodynamic energy dissipation in the circulation always impacts the pumping ventricle that, often always resulting in chronic heart failure as a secondary disease. For aortic stenosis, which is an arterial disease, an index based on total pressure (static plus dynamic) loss, which is a pseudo indicator of energy dissipation based on Bernoulli’s Equation, is widely used, while raw energy loss has been proposed to assess the severity of the Fontan connections clinically. Both diseases have separate frameworks for hemodynamic assessment of the respective dissipative lesions.

Numerous studies have shown that cardiac diastolic dysfunction and diastolic filling play a critical role in dictating overall cardiac health and demonstrated that the filling wave propagation speed is a significant index of the severity of diastolic dysfunction [1, 2]. However, the governing flow physics underlying the relationship between propagation speed and diastolic dysfunction are poorly understood. More importantly, currently there is no reliable metric to allow clinicians the ability to diagnose cardiac dysfunction on the basis of the wave filling speed.

Hemodynamic parameters such as time averaged wall shear stress (TAWSS), wall shear stress temporal gradient (WSSTG) and Oscillatory Shear Index (OSI) have previously been cited as parameters associated with the development of atherosclerotic disease at the human carotid bifurcation [1,2]. The sensitivity of these important parameters however, with variations of driving flow waveform, flow division and posture changes are not well known. To investigate these changes, we have used image based CFD, to analyze the flowfield of the carotid bifurcation of a healthy volunteer for five different input waveforms, three flow division ratios and two head postures.

The aim of this study is to develop a distributed model of the entire systemic arterial tree, coupled to a heart model and including a detailed description of the cerebral arteries. Distributed models of the arterial tree have been studied extensively in the past (Avolio [1], Stergiopulos et al [2], Westerhof et al [3]), however, no model has been developed so far that offers a physiologically relevant coupling to the heart and includes the entire cerebral arterial tree.

It is well established that atherosclerosis originates in low wall shear stress (WSS) regions near bifurcations and in curved segments of the coronary tree [1]. WSS also seems to influences plaque progression and destabilization, which explains the large interest in accurate assessment of the WSS.

There is much evidence suggesting that the initiation and progression of atherosclerotic diseases at the carotid bifurcation are influenced by “disturbed flow”. Although this term is not precisely defined, a variety of hemodynamic parameters have been proposed as indicators of disturbed flow, and some have been demonstrated to be more strongly correlated with biological responses.